Immunocompetent mouse model of endometriosis.

Yanfen Li (3239550), Malavika K. Adur (3239547), Athilakshmi Kannan (483347), Juanmahel Davila (787251), Yuechao Zhao (1358766), Romana A. Nowak (457413), Milan K. Bagchi (181461), Indrani C. Bagchi (181462), Quanxi Li (181459)
2016 · doi:10.1371/journal.pone.0165347.g001 · W6923201028
other OA: green CC0
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Researchers established an immunocompetent mouse model of endometriosis using uterine cell aggregates transplanted into ovariectomized recipients to assess ectopic lesion development under estrogen and progesterone treatments.

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This study utilized an immunocompetent mouse model to investigate the therapeutic effects of progesterone on endometriosis. Researchers transplanted uterine cell aggregates into ovariectomized mice and maintained lesions with estrogen, administering progesterone either before or after transplantation to assess its impact. The findings demonstrated that progesterone alleviates endometriosis by inhibiting uterine cell proliferation, reducing inflammation, and suppressing angiogenesis within the ectopic lesions. This paper is centrally about endometriosis — specifically the mechanistic role of progesterone in treating established lesions using an immunocompetent mouse model.

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Abstract

6–8 weeks-old CD1 female mice were primed with PMSG for 48 hours. Uterine tissues were then harvested and minced into tiny cell aggregates after myometrial removal. Female mice with the same genetic background were subjected to ovariectomy and served as recipients. 2 weeks after surgery, equal volumes of uterine cell aggregate suspension were transferred into the peritoneal cavities of recipients. Endometriosis was maintained by subcutaneous administration of 100 ng of E2 once every 4 days until tissue collection. For the studies of the role of P4 in endometriosis, 1 mg of P4 (pre-P4) was administrated along with E2 beginning at 4 days before transplantation. For P4-resistance experiments (Post-P4), 1 mg of P4 was administration along with E2 beginning at 4 days after transplantation. The ectopic lesions were assessed under a dissecting microscope at different days after endometrial cell transplantation (n = 6 per treatment group).
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Progesterone Alleviates Endometriosis via Inhibition of Uterine Cell Proliferation, Inflammation and Angiogenesis in an Immunocompetent Mouse Model Fig 1 Immunocompetent mouse model of endometriosis. 6–8 weeks-old CD1 female mice were primed with PMSG for 48 hours. Uterine tissues were then harvested and minced into tiny cell aggregates after myometrial removal. Female mice with the same genetic background were subjected to ovariectomy and served as recipients. 2 weeks after surgery, equal volumes of uterine cell aggregate suspension were transferred into the peritoneal cavities of recipients. Endometriosis was maintained by subcutaneous administration of 100 ng of E2 once every 4 days until tissue collection. For the studies of the role of P4 in endometriosis, 1 mg of P4 (pre-P4) was administrated along with E2 beginning at 4 days before transplantation. For P4-resistance experiments (Post-P4), 1 mg of P4 was administration along with E2 beginning at 4 days after transplantation. The ectopic lesions were assessed under a dissecting microscope at different days after endometrial cell transplantation (n = 6 per treatment group).

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endometriosis

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